S6K is a serine/threonine kinase that is a member of the ribosomal S6 kinase (RSK) family. S6K exists in two main isoforms, S6K1 and S6K2, which can also be alternatively spliced to produce different splice forms. S6K1 has two major splicing products that are approximately 70 kDa and 85 kDa, known as p70S6K and p85S6K respectively. S6K is activated via phosphorylation by mTORC1 which relieves the autoinhibition of S6K. Active S6K phosphorylates the ribosomal S6 protein, which induces protein synthesis and cell growth and proliferation. S6K also phosphorylates EIF4B and EEF2K to upregulate protein synthesis. Many binding partners of S6K have been identified and indicate many roles for S6K in cellular growth, proliferation, and survival. S6K also plays a role in a negative feedback loop for mTOR signaling by phosphorylating RICTOR (1). RICTOR directly inhibits mTORC2 and AKT1 which ultimately impedes mTORC1 signaling.
Le et. al. used the phospho-S6K antibody (p Thr421) to assess how Paclitaxel, a widely used chemotherapy, affects S6K activity in breast and ovarian cancer cell lines (2). The group used the S6K antibody to assess phosphorylation states of S6K during treatment with Paclitaxel. The S6K antibody showed that Paclitaxel treatment induced phosphorylation of S6K at Thr421 and Ser424 in a time and concentration-dependent manner. Phosphorylation at these sites inhibits S6K signaling, preventing movement through the cell cycle and ultimately leading to cell death.
Meanwhile, Rhoads et. al. used the S6K antibody to study the role of S6K in Rotavirus Enteritis using a piglet model of the disease (3). Rotavirus Enteritis is a common form of infectious diarrhea that affects millions of people each year and accounts for many hospitalizations and healthcare costs. The group used the S6K antibody to assess total levels of S6K in jejunal cells of infected and control piglets. The results showed a sharp increase in S6K levels and activation in the infected cells, indicating activation of protein synthesis during this mucosal injury. The group identified mTOR signaling as the upstream activator of S6K in this condition. They suggest that amino acid supplementation may be a beneficial treatment to further promote protein synthesis and intestinal repair during acute Rotavirus Enteritis.
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